Cardio 1 Flashcards

1
Q

What medication is indicated in treating torsades de pointes?

A

IV Mag Sulfate is used for the treatment of polymorphic VTach assoc with acquired QT prolongation.

** Not used in VF from MI

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2
Q

How would you manage a Pt with VFib vs Afib/Aflutter?

A

VFib or pulseless VTach should be managed with immediate defibrillation.

In Pt with hemodynamic instability due to Afib, Aflutter, or VT with a pulse should be managed with synchronized cardioversion.

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3
Q

What drug would you use for a patient with intermittent claudication?

A

Cilosatzol (phosphodiesterase inhibitor) can be used for symptomatic management of a Pt with intermittent claudication.

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4
Q

How does sublingual nitrate provide symptomatic relief in stable angina?

A

Nitrates cause direct smooth muscle vascular relaxation&raquo_space; systemic venodilation and ^ peripheral venous capacitance. Anti ischemic effect is due to systemic venodilation&raquo_space; decrease in cardiac preload&raquo_space; decrease in end diastolic and end systolic volume&raquo_space; decreased LV systolic wall stress&raquo_space; decreased oxygen demand&raquo_space; improved symptoms.

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5
Q

A holosystolic apical murmur radiating to the axilla would be pathognomonic for …

A

Mitral Regurg

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6
Q

A 2/6 systolic ejection murmur at R sternal border and LVH would indicate …

A

Aortic stenosis

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7
Q

In which cases would you use direct current cardioversion vs defibrillation vs transcutaneous pacing?

A

Defibrillation - provides high energy shock at a random point in the cardiac cycle (unsynchronized shock) and is indicated in patients with V-fib or pulseless V-tach.

DC Cardioversion - energy synchronized to the QRS complex to minimize shock during repolarization (may precipitate V-fib). Should be given to patients with persistent tachyarrhytmia causing hemodynamic instability.

Transcutaneous pacing - symptomatic bradycardia and complete heart block.

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8
Q

What is the MOA of dobutamine in HF?

A

Dobutamine - adrenergic agonist (predominant activity with B1-AR) and minimal activity of B2 and alpha 1 R. Has positive inotropic and chronotropic effect. Stimulation of B1&raquo_space; ^ cAMP production in cardiac myocytes&raquo_space; ^ Ca2+ mediated binding of actin-myosin to troponin C&raquo_space; ^ myocardial contractility (positive inotropic effect)

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9
Q

Auscultation finding of mitral regurg:

A

holosystolic murmur at cardiac apex radiating to axilla.

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10
Q

Auscultation findings of mitral stenosis:

A

diastolic rumble heard at cardiac apex.

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11
Q

Auscultation findings of mitral valve prolapse:

A

nonejection click with mid-to-late systolic murmur. Due to myxomatous degeneration of mitral valve leaflets

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12
Q

What therapy would you use for a patient in sustained monomorphic V-Tach who are hemodynamically stable?

A

These patients can be initially managed with antiarrhythmic drugs. IV Amiodarone is the preferred agent. Procainamide, sotalol, and lidocaine are secondaries.

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13
Q

How do you treat paroxysmal supraventricular tach (PSVT)?

A

carotid massage.

Hemodynamically unstable VTach gets synchronized cardioversion. Vfib and pulseless VT should get defibrillation (unsynchronized shock).

** Digoxin is used for supraventricular arrhythmias (atrial flutter, atrial tach, A-fib) especially in people with HF who aren’t able to tolerate BB or CCB.

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14
Q

What is the MOA of statins in treating hypercholesterolism?

A

Statins inhibit HMG CoA reductase, which is responsible for converting HMG CoA to mevalonate&raquo_space; decreased hepatic cholesterol formation&raquo_space; activates cell signaling to increase # LDL R on liver cell membranes&raquo_space; ^ removal of circulating LDL

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15
Q

What is a primary side effect of statins?

A

Statin induced myalgias. Statins can cause proximal symmetric muscle weakness because they decrease CoQ10 synth which is involved in muscle cell energy production.

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16
Q

Would you have increased or decreased renal venous pressure in case of systolic CHF and reduced CO?

A

You would have reduced CO and increased renal vascular resistance due to activation of sympathetic system and RAAS.

17
Q

What’s the major clinical presentation of a Pt with scleroderma renal crisis?

A

Sudden onset renal failure (without previous disease) and malignant HTN (blurry vision, HA, nausea). Likely due to increased vascular permeability + coag cascade activation + increased renin secretion.

18
Q

Beck’s Triad:

A

hypotension, distended neck vein, muffled heart sounds.

Characteristic of cardiac tamponade.

19
Q

What pharmacologic agent prevents ventricular remodeling after MI?

A

ACEi